Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin signaling and carbohydrates… Part II(d)

When last I left off, the subject of discussion was the critical question about the food reward/palatability hypothesis of obesity: Can palatability and reward value of foods be disassociated from the metabolic and hormonal effects of the individual nutrients being consumed and, in particular, the sugar and refined grains that “hyper-rewarding” foods seem to invariably contain?

Let’s start with the experiment in humans that Dr. Stephan Guyenet of wholehealthsource.org finds such compelling support of the food reward hypothesis. This was work done by Ted Van Itallie and Sami Hashim back in the 1960s. (For an idea of the simplistic notions held by Dr. Hashim about obesity and its cause and prevention, I highly recommend this video here. I discuss Dr. Van Itallie’s critical role in shaping the current thinking about obesity — i.e., the mess we’re in today — in chapter 23 of Good Calories, Bad Calories.)

In his “Case for the Food Reward Hypothesis of Obesity, Part II” post, Dr. Guyenet argues that this experiment is important because it demonstrates what he considers one of several critical requirements for the validity of the food reward hypothesis: “Decreasing the reward/palatability of the diet should cause fat loss in animals and humans that carry excess fat.” Here’s what he says:

One of the most striking weight loss studies I’ve seen was conducted in 1965 and involved feeding a bland liquid diet through a dispensing straw (12). Lean and obese volunteers were instructed to eat as much of the liquid food as they wanted, but they were permitted no other food. While lean volunteers ate a normal amount of calories and maintained weight, obese volunteers dramatically reduced their spontaneous calorie intake and lost fat rapidly, with one man losing 200 lbs in 255 days without hunger. This is exactly what one would expect if unpalatable/unrewarding food lowered the biologically “defended” level of fat mass. Interestingly, the diet was high in sugar but was otherwise very low in palatability/reward value.

This was Dr. Guyenet’s second discussion of the tube-feeding paper. As he explained in an earlier post on this experiment, the total number of subjects was four: two lean and two obese. The two lean were kept on the feeding machine for 16 and 9 days. They didn’t bother to decrease caloric intake, and so their experiment ended then. The two obese subjects, however, curtailed intake dramatically, to 275 calories per day for the male volunteer and 144 for the female). The man stayed with the feeding machine for another 70 days and was then sent home with the formula and the instruction to drink only 400 calories a day. He kept this up for another half year until he had lost the 200 pounds. Says Dr. Guyenet (in “Food Reward: a Dominant Factor in Obesity, Part II”, his earlier post):

This machine-feeding regimen was nearly as close as one can get to a diet with no rewarding properties whatsoever. Although it contained carbohydrate and fat, it did not contain any flavor or texture to associate them with, and thus the reward value of the diet was minimized. As one would expect if food reward influences the body fat setpoint, lean volunteers maintained starting weight and a normal calorie intake, while their obese counterparts rapidly lost a massive amount of fat and reduced calorie intake dramatically without hunger. This suggests that obesity is not entirely due to a “broken” metabolism (although that may still contribute), but also at least in part to a heightened sensitivity to food reward in susceptible people. [The italics are mine.]

So immediately we have a problem, and it strikes me as near-fatal for the food reward hypothesis of obesity. In Dr. Guyenet’s first post on the experiment (the one immediately above), he says that the regimen “was nearly as close as one can get to a diet with no rewarding properties whatsoever…. It did not contain any flavor or texture to associate them with, and thus the reward value of the diet was minimized.” In his second post (the first of the two I quote, just to make life confusing), he notes that the diet was “high in sugar” although he tries to hold onto the food reward hypothesis by stating that it “was otherwise very low in palatability/reward value.”

This is why I asked Dr. Guyenet at the AHS whether the formula diet had sugar in it. If it did, then how could it be bland? And how could it have a low food reward value, which is, more or less, the whole point? It might have a lower food value than what the two obese subjects were eating prior to the experiment, but low?

As Hashim and Van Italie noted in a footnote in their 1965 paper, and as Dr. Guyenet notes in his blog, the formula used was Nutrament. This was a liquid diet formula that went on sale in 1960 (according to Wikipedia), and if the composition then was anything like the composition now, a significant portion of the carbohydrate calories came from sugar.

So was it non-rewarding? Hashim and Van Italie refer to it as “bland” and Guyenet assumes it was as well, hence his description of it as “otherwise very low in palatabily/reward value.” But it had to be sweet if it had significant sugar in it; and indeed in the modern incarnation of Nutrament, which may or may not be the same as the original, there are 47 grams in every 12-ounce serving. This happens to be more sugar than you’d find in a 12-ounce can of Coke.

Frankly, the stuff sounds awful, but low in reward value? Well, only if a Coke is, too, and certainly not if Dr. Guyenet includes “liquid calories, particularly sweetened beverages” among the low-hanging fruit of the food reward hypothesis, which he does.

In fact, the point of a diet formula like Nutrament is not just that it contains enough protein and other nutrients that people can thrive on, say, 400 or 800 calories-a-day of the stuff. But it also has to taste good, so that consumers will continue to buy it and drink it day in and day out, even after they’ve moved into the weight maintenance phase of their lives — i.e., for the rest of their lives. It’s an example from the 1960s of what Dr. Guyenet describes as “the goal of processed food manufacturers… to create a product that maximally reinforces purchase and consumption behaviors—food reward!”

We can try to get around this problem by suggesting that bland and sweet is just not high in food reward value, as Dr. Guyenet tries to do, but we’re going to resort to this kind of, well, blatant contradiction only because we want to salvage this experiment as support for the hypothesis. So this formula must have a low-food reward value because an obese subject consumed less of it and lost weight and because we believe that foods with high reward value cause people to gain weight. Now we’re back to circular-definition land, a place I would prefer to never visit.

Now, how about the idea that a “cafeteria” or “junk food” diet makes humans and animals fat, a concept that was pioneered by Anthony Sclafani. The assumption is that such a diet is fattening because there’s something about eating a variety of foods, mostly junk foods, that is so rewarding or at least so less bland than a plain chow diet that both humans and animals get fat eating it. Here’s how Dr. Guyenet describes it:

Aside from Dr. Guyenet’s description of standard rat chow as “whole-food based,” my major problem with this (which is the same problem Ramirez et al had 20-odd years ago with the existing research then) is that this is an experiment that changes an unholy host of variables, and the results are evoked to make a point about one: food reward value.

One advantage I have in this nutrition business as an arguably ignorant journalist is that I actually get to interview the researchers who do the work. (Technically anyone could do this, but the researchers are certainly more likely to give their time to a journalist, ignorant or not, than to what one of my acquaintances in academia refers to as “just a person.”) I interviewed Sclafani back on January 30, 2003 for GC,BC, and the interview revealed the obvious problem with this interpretation. As Sclafani told me, they started their cafeteria diet (which he was calling the “supermarket” diet at the time) with a variety of different foods (not quite as wide a variety as Dr. Guyenet is discussing above, but wide nonetheless): chocolate chip cookies, salami, cheese, bananas, marshmallows, milk chocolate, peanut butter and sweetened condensed milk, and then they later simplified it to four foods because the rats didn’t eat all the foods they gave them.

Which foods did they ignore? Sclafani said they never did a systematic study, nor had anyone else, as far as he knew (as of January 2003), but cheese, salami and peanut butter—the foods highest in fat and lowest in refined grains and sugar—seemed to be the foods they avoided in favor of the sweeter, starchy options. So the obvious question: are refined grains and/or sugar necessary to impart not just reward value, but reward value that leads to people and animals getting fat?

In fact, Sclafani told me that they had based their selection of foods on a hunch about what rats preferentially like, and so that’s why they included cheese in the list. It seemed like an obvious choice. After all, don’t you stick cheese in mouse traps when you want to rid your house of mice? And yet, cheese was not among the foods the Sclafani’s rats preferentially ate when given all these other refined carbs and sugary foods to eat instead. Maybe because the cheese was unrewarding. Or maybe because it was relatively if not completely refined-carb and sugar free, as were the salami and peanut butter.

This inability to differentiate food reward and/or palatability from the presence of refined carbs and sugars haunts virtually every example of the studies cited to document food reward and/or palatability.

Another example, not one used by Dr. Guyenet, is Kelly Brownell’s Yale Food Addiction Scale . This scale attempts to identify people who suffer from addiction to certain foods. The scale is based on a survey that gives a series of statements about eating habits. Subjects must say how true each statement is, on a scale from “never” to “four or more times or daily.” This goes along with a list of foods of which food addicted subjects might have “difficulty controlling their intake.” Here are the first four statements to give you an idea of what Brownell is getting at:

I find that when I start eating certain foods, I end up eating much more than planned.

I find myself continuing to consume certain foods even though I am no longer hungry.

I eat to the point where I feel physically ill.

Not eating certain types of food or cutting down on certain type of food is something I worry about.

So let’s assume, for the sake of argument at least, that the “certain foods” that illicit addictive behavior is very similar to the list of hyper-rewarding foods, the ones most likely to cause obesity. Here’s Brownell’s list of the foods that are most likely to be addictive:

With the exception of steak and bacon, all of these foods are high in carbohydrates — refined or otherwise (the French Fries) — and/or sugars, even the foods defined as “fatty” with the aforesaid exceptions. If these foods are addictive and if they cause obesity, is it because they’re addictive or is it because of the metabolic and hormonal effects of consuming them — their effects on insulin signalling? There’s no way to tell without an exceedingly well-controlled and well-conceived experiment, but you can guess where my vote lies.

What about the steak and bacon, then? Well, if you ate nothing but those—steak and bacon every day, plus, say, the hamburgers or cheeseburgers without the refined grains attached, i.e., the buns—you’d be eating a weight loss diet (a ketogenic diet) and would almost assuredly lose weight doing it. So whether or not you consider steak and bacon addictive, it’s unlikely that they could be defined as foods high in reward value because they would tend to refute the hypothesis that high food reward value causes obesity. And now we’d be back to this problem of having to differentiate between hyper-rewarding foods or at least addictive foods that come with refined/easily digestible carbohydrates and sugars and cause fat accumulation and hyper-rewarding foods that don’t, and well, don’t.

Of the examples I could find in Dr. Guyenet’s discussions of the food reward/palatability hypothesis that held the promise of differentiating food reward value from underlying metabolic effects of the foods themselves (and the presence of refined or easily-digestible carbs and sugars), none of them actually came through with meaningful evidence.

The studies most likely to offer such a differentiation were those mentioned by Dr. Guyenet in his post, “The Case for the Food Reward Hypothesis of Obesity, Part II.” These were the studies evoked as evidence for the hypothesis because they demonstrate that “Individual sensitivity to food reward should predict future fat gain.” About this evidence he says:

I’m aware of three studies that have investigated this question. In the first, researchers found that the reinforcing value of food relative to a non-food stimulus predicted fat gain over the next year in 7-10 year old children (19). In the second, the responsiveness of reward-related brain regions to imagining palatable vs. unpalatable foods (as assessed using fMRI) predicted body mass index (BMI) gains in adolescent girls, and this effect was modified by gene polymorphisms in dopamine receptor genes (20). The third study also used fMRI to demonstrate that greater activation in reward-related brain regions during exposure to appetizing food cues predicted greater BMI gains over time in adolescent girls (21).

But of those three studies, none of them define what the high reward foods were, which foods were considered palatable and which were unpalatable. For all we know, the palatable foods were the ones rich with refined grains and sugars and the reason reward-related regions of our brain light up when we eat them (or at least when obese people do) is because our brains are responding to what these foods do to our bodies.

Reference 19 doesn’t specify at all which foods are actually high in reward value, nor do references 20 and 21, which are both by the same authors. They do, however, include a “cheeseburger” as an example of a processed food, demonstrating a certain bias against cheeseburgers that may be misplaced.

And reference 21 says that while BMI may have been related to the extent of activation in reward-related brain regions, as Dr. Guyenet points out, this was true regardless of whether the food being imagined was rewarding or palatable or not. Or the authors put it, “BMI [body mass index] was positively correlated with behavioral response to both appetizing and unappetizing food images, implying that food cues in general trigger greater attention in overweight vs. lean individuals.”

One obvious interpretation is that overweight individuals are hungrier than lean individuals, and so they have a greater response to any food in their reward centers. And, in fact, one point Dr. Guyenet’s mentor, Michael Schwartz, made of interest in his 2006 review in Nature “Central nervous system control of food intake and body weight” was that “food deprivation strongly augments the reward value… reduced food availability seems to exert a global, stimulatory effect on reward perception.” And so maybe the greater the BMI, the more likely the subjects were hungry or food deprived—a phenomenon I discuss at length in GC,BC— a state that could be due to increased insulin secretion and chronic hyperinsulinemia. And maybe refined grains and sugars augment reward value because they cause us to secrete more insulin and store calories away as fat and glycogen and make us hungry.

In GC,BC I quote Mark Friedman commenting on this potential carbs-insulin-hunger connection regarding just the cephalic phase of insulin secretion, the one that comes just by thinking about a particular food:

This cephalic release of insulin also serves to clear the circulation of “essentially anything an animal or a person can use for fuel. Not just blood sugar, but fatty acids, as well. All those nutrients just go away.” Hence, the thought of eating makes us hungry, because the insulin secreted in response depletes the bloodstream of the fuel that the peripheral tissues and organs need to survive.

And if this happens more in individuals who are insulin resistant, as most obese individuals are, we’re now back at a hypothesis that maybe the insulin signaling in the body is running the brain’s response, not vice versa. Yes, it’s the brain that’s stimulating the insulin secretion when we think about food, but what makes us hungry and makes the food then seem so rewarding is the effect of the insulin secreted in the body.

Comments

It seems there major issues is that the definition of a ‘palatable’ food is circular. That is, if someone eats it to excess then it’s palatable. If they don’t eat it to excess, it’s not palatable – regardless if it’s macronutrients.
It also also seems that this conflict could be resolved by making a ‘cafeteria’ of palatable low-carb foods (peanut butter, avocado, lard, butter, cheese, etc.) for 1 group of rats (assuming ‘palatable’ is not a synonym for ‘sugary’), and then giving a separate group of rats a ‘cafeteria’ of high-carb food (cookies, cake, etc.) and see which group gets fatter. And comparing both rat ‘cafeteria’ groups to a control group on normal rat chow seems like an elegant solution.
Would you make any changes to this experimental setup if Dr. Guyenet seeks to differentiate food-palatability from simply high-carb food?

> “It seems there major issues is that the definition of a ‘palatable’ food is circular. That is, if someone eats it to excess then it’s palatable. If they don’t eat it to excess, it’s not palatable”

It seems to me that “palatable” has a clear meaning. I think that it is not for S. Guyenet to re-define it. By any reasonable meaning of the word “palatable”, standard French fare is more palatable than standard US fare, yet the French do not over-eat so much as do those in the US.

You, David Gilmore, may find that “standard French fare is more palatable than standard US fare”. But, I am sure that many, if not most, Americans would NOT find it palatable, let alone “rewarding”, and the same would apply to the French and the SAD. Palatability like ANY taste, and/or sense of beauty, is in the eyes (mouth) of the beholder.

I agree entirely that “If S. Guyenet wants to be clear, he should choose a different word.” I think
“reward” and “palatable” are useless regarding overeating and obesity. The obese people I know would agree – they ALL say that unconscious eating is their problem. They sit down to watch TV with a BIG bag of potato chips and are surprised to find that it is empty – they ATE THE WHOLE THING, all of the chips, with little, if any, awareness. And they repeat this with chips and other food regularly, if not daily.

“But, I am sure that many, if not most, Americans would NOT find it palatable, let alone “rewarding”,

Indeed, terrence, which is why American food critics and ordinary people alike spit at the mention of Le Bernadin, why French Laundry and Per Se are constantly rated among the worst restaurants in America, and no one, but no one, ever bought Julia Child’s cookbooks. Yes, I agree – Americans would rather eat living, squirming maggots than French food. Because it’s just that “unrewarding.”

Exactly who do you think you “agree” with BlueEAyesSF? And what if those restaurants and cook books are popular – do you really think the majority of Americans eat that way.

Exactly who said “Americans would rather eat living, squirming maggots than French food. Because it’s just that “unrewarding.”?” I do not, and if you read my comment you would know I did not. If it is an attempt at humor, you failed miserably. snort!

Very, very minor note: “Froot Loops”, with the misspelling, is the actual name of a Kellogg’s product. It contains nothing obviously recognizable as fruit (perhaps the misspelling is for legal reasons?), but the very first ingredient is sugar; see http://www2.kelloggs.com/ProductDetail.aspx?id=566

It seems like you’re suggesting that either insulin itself is an addictive drug, unleashed by the consumption of refined / high-GI carbs; or that the rush that comes when you eat sugar after the insulin surge has cleared all the energy out of your blood in preparation is addictive; or both. Am I reading that correctly?

In any event, the notion that there’s something addictive about the impact of high-GI high-carb food is certainly in line with my personal experience.

Great pickup on the Fruit versus Froot. Hadn’t ever picked up on that.

I don’t want to speak for Gary, but from my POV, the insulin surge is not an addictive signal; it’s a normal anticipatory/physiological response to a bolus of glucose coming our way. Fatsos have it worse for metabolic reasons.

I agree with Stipetic (although I rather not be called a “fatso” )that insulin per se is not addictive, and while many may experience a feel-good “sugar rush”; I think the real impetus to overeat here (as I understand Gary keeps saying) is hunger. [Abnormally] raised insulin levels quickly locks energy away leaving the cells starving and crying out for more of the same fast energy foods.

The diabetic who injects too much insulin experiences this as an hypo when the body cries out for fast sugars (it really is an intense drive to eat)… I don’t see it as a stretch to imagine the same kind of drive to eat fast sugars, occurring to a less acute extent but over many days, weeks, months and years of raised insulin levels.

Your concluding remark was what I was trying to convey with my Chunky Monkey comment in the last thread, but you made it more eloquently, if not more scientifically (and didn’t overuse “hey” in doing so). With the advent of free Pubmed access, the internet has been inundated with Pubmednonites citing this and that study in support of such and such point of view. It’s nice to have the cherry picking/pickers pointed out. That’s for helping out, Garry.

You are mistaken. The times in my life when I gained fat were times when I ate a lot of carbohydrate and very little fat. I now stay thin on very little carbohydrate and lots of fat, which does not fit into your two categories, so perhaps they do not include “all of us”.

Eating fat does NOT make people fat. Eating a lot of (processed) carbohydrate makes people fat.
The obese people I know do NOT eat much, if any, fat as a part of what they eat; they purposely avoid eating fat, under the mistaken view that it is not healthy to eat fat. They eat sweet carbs, lot of them.

I have seen clinical studies of mice that show that mice prefer water with sugar in it OVER water with cocaine it – even after being made addictive to cocaine. Guess what – they ALL got fat. And they all drank much more sweetened water they was required to keep them hydrated.

Tom….I Disagree completely… my life as a very fat person.. starting as a fat child in a skinny, meat and fat phobic family and as an adult hovering at 300 lbs. was spent eating nearly no fat, very little protein and mostly carbs of all kinds.. Typically breakfast was sweetened cereal with “blue milk”, and juice, lunch was peanut butter and jelly on white bread with fruit and maybe some sort of sugary treat and juice.. snacks of more cereal and skim milk or juice and a dinner with some meat and loads of pasta, potatos, or rice and corn or peas and juice. I carried these bad eating habits into adulthood. I lived a life of constant hunger, preoccupied with thoughts of food, feeling driven to eat and never feeling satisfied even though I felt stuffed… I also felt lethargic and slept more than I should. My binge eating tended to be bags of “fat free” candy and huge bowls of rolled oats made with water, artificial sweetener or sugar and cinnamon.
Fast forward to 50 years old…. After 4 years of a very low carb, moderate protein and high fat paleo way of eating… I am over 120 lbs lighter, full of energy, very active, after a solid eight hours of sleep I wake refreshed and ready for my busy, happy life. Does sugar, and too many carbs in general, make me fat…yes!

Reward has to be part of my food problem. If I had no food that I liked, I would lose some weight, on the other had, I will overeat if the food is good and novel in taste. But these are short term effects. The impact decreases with time.

Reward is the starting point. After the liver and muscles are topped up with glycogen, insulin resistance starts to push glucose into the fat cells. Now insulin is in control. We need both Reward and insulin to gain, but to lose, the only way is just food shortage of some form. Some of you have a preconceived notion of how much meat to eat, and if that works, good for you. I, on the other hand, gain weight on steak and bacon.

The only way I can lose weight is by controlled low carb meals. I have a long list of things that are part of my obesity problem. Your work has been part of my solution. Thank You.

Dr Guyenet is attempting to use “Food Reward” as a scientific term, and has no way to define or test the quantitative nature of this term. It is like “Beauty” or “Artistic Quality”, something you “Know When You See It”. Naturally, this falls into great difficulty, as it means different things to different people, and can mean different things to the same person at different times.

In this qualitative sense, I can agree that ‘food reward” in the form of salt, fat and carbohydrates (specifically the various sugars and sugar-like substances) is generally Associated with obesity in a statistical sense. However, this does not constitute causation.

The classic example is the well established Association between the number for firefighters at a fire and the physical damage resulting from the fire. This is a good Association, and some attempt to use this association to conclude that the large number of firemen are the Cause of the greater damage (from more chopping of holes in the building and extra flooding of the structure with damaging water and….).

In actuality, the above explanation ignores the physics of a fire. Unless a fire is controlled pretty promptly, the damage is greater because the fire gets more intense before the turning point is reached by the actions of water. In order to promote faster reduction of the blaze, when a fire is either already very large or has potential to easily become large, the logical approach is to call out large numbers of firefighters and firefighting equipment. So the real and/or potential size of the fire (and resulting damage) is the reason for the call out of many more firefighters and firefighting vehicles.

Yes, there are people who appear to believe that the damage is caused by the large number of firefighters. But, it is not the majority opinion, at least I so hope.

Obesity is a contentious subject, and perhaps using obesity phenomena as a matter of clarification, it mainly causes confusion instead.

So we will discuss poison instead as it is much simpler.

Imagine substance X, which in small doses has some modest unspecified health benefit. However, in large quantities consumed over a long period of time, is toxic – frankly poisonous. However, substance X tastes bad.

To promote sales of substance X, the manufacturer simply attempts to raise the ease of consumption by increasing the food reward by some combination of fat, salt and sugary carbohydrates. And, this works.

Sales grow and consumption of the “healthy” component substance X increase. Unfortunately, consumers ignore the cautions of excess consumption (like, say, determined cigarette smokers), and consume unhealthy amounts of substance X. They then get ill and there are some fatalities.

Is the “Cause” of illness and death the high food reward or the basic toxicity of substance X?

What would Dr. Guyenet likely conclude, and what would Mr. Taubes conclude?

I would go with the Cause of death was toxicity of substance X, and the Enabler of the episode of death and/or illness was the higher food reward of the marketed product.

Not everything that plays a role in an outcome is actually a Cause… but many things may Contribute or Enable.

Nicotine may not be the poison or toxin which causes the tissue damage of cigarette smoking. However, if you think about it Nicotime imparts a “High Breathing Reward” aspect to cigarette (and tobacco) consumption (smoked).

So, should I postulate that the cause of tissue disease associated with cigarette smoking is CAUSED by the “High Breathing Reward” or should I consider that the Enabler of the tissue damage in smokers is the “High Breathing Reward” of the nicotine flowing into the lungs, carrying with it a number of toxic tissue damaging chemicals?

I again wonder what Dr. Guyenet would conclude and — well I pretty much can guess what Mr. Taubes would conclude.

It might also be worth pointing out that the poor folks on the bland-feeding-tube-diet were consuming Atkins-induction level carb intake. At “275 calories per day for the male volunteer and 144 for the female” — these people clearly went into ketosis and started burning their own fat for fuel. They were basically doing hard core Atkins.

I saw Guyenet’s presentation at AHS. He made no mention that these tube-feeders were eating at Atkins-induction-level. Why not?

On a grander note: I propose that it’s high time the low carb / paleo world finish up its dithering over FW and other such memes and just accept that Gary and Lustig are correct about the whole calories-in-calories-out thing being BS.

ENOUGH. Gary and Lustig are right about calories. Dr. Hashim’s YouTube presentation is mindless drivel that must be eradicated if America is going to survive. We don’t need Guyenet or anyone else confusing this issue. (If we want to debate the biochemistry at length — including the roles of insulin, leptin, LPL, “palatability” and the like — that’s of course fine. Not trying to smother dissent here.)

Calories-in-calories-out is the Emperor. It is the glue that holds all the B.S. together.

The Food Pyramid (or Plate, or whatever) is Darth Veder.

The questions for the low carb/paleo world are stark and clear:

a) Do you want to defeat Darth Veder?
b) If so, are you ready and willing to take down the Emperor? Because if not, you’re either not making a dent or you’re abetting the enemy.

“in the modern incarnation of Nutrament, which may or may not be the same as the original, there are 47 grams in every 12-ounce serving. This happens to be more sugar than you’d find in a 12-ounce can of Coke.”

You realize Coke also has a very strong non-sugar flavor right? And other things to make it hyper-palatable.

Seth Roberts and his disciples claim to lose a lot of weight by adding sugar water to their diets. They claim this is because sugar water has very low reward value. Notice that even pixie stix have added flavor and color to make them more appealing. Lastly, few people gorge themselves on spoonfuls of plain sugar. I think it is pretty clear that sugar in and of itself is not rewarding / hyperpalatable.

Kit, It’s not just the reward in the taste, but the biochemical effect high GI foods have in the brain’s reward centres, that like opiates, gives the “reward” from eating them. And I’ve seen my niece down spoonfuls of sugar, under her mothers gaze, despite the fact I tell her one day she might have to have her feet cut off because of it…

“So was it non-rewarding? Hashim and Van Italie refer to it as “bland” and Guyenet assumes it was as well, hence his description of it as “otherwise very low in palatabily/reward value.” But it had to be sweet if it had significant sugar in it; ”

Gary, this argument sounds like an argument my philosophy professor made when discussing the Euthyphro Dilemma in the first lecture of a moral philosophy class I took my sophomore year of college (an argument, which, after hearing him try to defend, caused me to immediately log into the registrar office website and figure out how to change my grading option on this class to pass/fail because I knew I wasn’t going to be attending any future lectures). The question of the dilemma is whether that which is good is moral because god made it so or whether god made it that way because it is inherently good. Ignoring god for a second, because the dilemma exists outside of the framework of a deity, he used the fact that killing puppies is self evidently immoral as a refutation of the position that things are moral because god says so.

Like my professor, you are asserting that it is self evident that sugar is hyper-rewarding. The problem, of course, is that not only is this not self evident, but it isn’t even supported by the literature. In other words, to answer your question, the fact that it has sugar in it is not sufficient evidence that it is hyper-rewarding. Coca-Cola has a list of ingredients that is at least 9 distinct substances long, how did you single out sugar as being the one that is hyper-rewarding? I would go as far as to say that the fact that sugar made up a large percentage of the bland liquid diet is definitive proof, in and of itself, that sugar is not inherently hyper-rewarding. It’s the black swan in your theory that all swans are white.

“With the exception of steak and bacon, all of these foods are high in carbohydrates — refined or otherwise (the French Fries) — and/or sugars, even the foods defined as “fatty” with the aforesaid exceptions. If these foods are addictive and if they cause obesity, is it because they’re addictive or is it because of the metabolic and hormonal effects of consuming them — their effects on insulin signalling?”

The problem with this line of questioning is that bacon and steak are are low carb, meaning that they are missing an enormous part of the reward value puzzle. To swing it to the other side, let’s take a look at french fries. A quick lookup of the nutrition facts of McDonalds french fries would show you that they have a near 1:1 carb:fat ratio by calories. So are french fries high carb or high fat? Or maybe it is the combination of carbohydrate and fat, or carbohydrate and artificial sweetener, or fat and artificial sweetener, that makes these foods hyperrewarding. Or maybe I’m wrong, and it’s just the refined carbohydrates. If that were the case, we would expect that foods that are high in carbohydrate but low in fat to be fattening.

“What about the steak and bacon, then? Well, if you ate nothing but those—steak and bacon every day, plus, say, the hamburgers or cheeseburgers without the refined grains attached, i.e., the buns—you’d be eating a weight loss diet (a ketogenic diet) and would almost assuredly lose weight doing it. ”

The same can be said for high carb, low fat foods like potatoes or plain white rice. If you ate nothing but those—potatoes and other very low fat starch sources every day—you’d be eating a weight loss diet, and would almost assuredly lose weight doing it.

I should have added that Diet Coke, which has no sugar in it, is almost definitely hyperrewarding as well. This property of it does a better job of explaining why some people, particularly the obese, break through plateaus in their weight loss when they remove diet sodas and other artificial sweetener sources from their diet than your “sweet tastes spike insulin and cause fat storage” explanation.

Diet sodas often contain aspartame – aspartic acid is a break down product – it not only hits the same glutamate receptors as MSG, it is easily turned into glutamate in the body. Glutamate is then turned into GABA which hits the same receptors as valium. The problem is that glutamate also causes the pancreas to release a flood of insulin. If you wanted the make an obese person even more hungry – starve them of carbs and hit that insulin button to clear what little blood sugar was around. Why do you think the food industry uses glutamate and aspartame? It isn’t because they care about you. They only care about what keeps you eating more.

Carol, do you have a good reference for the metabolic pathways aspartame follows? What type of insulin response aspartame elicits relative to sugar? I have an unfortunate addiction to diet sodas (and, yes, I do actually crave the stuff) and I wouldn’t mind to read up on some valid literature on the subject.
Incidentally, after watching Taubes GoogleTalk earlier this year, I eschewed carbohydrates fairly utterly, I’d say, and I have experienced exceptional results (drastic weight loss, increased energy levels, reduced appetite), yet I still drink litres of diet soda every day. Anyone notice omitting artificial sweeteners from their diets helped them shed lbs?

I haven’t drunk Coke in decades, but from what I remember, it’s not exactly the sweetness that gets you, it’s a kind of bitter-sweet impact on your tongue. It’s similar with some beers, although perhaps they tend more towards the bitter than the sweet.

Gary,
As many have before me, thank you for these posts. Have greatly enjoyed your work on this topic, especially your evisceration of the mainstream science in regards to diet and obesity. As you have a physics background, I would like to see your take on the state of astrophysics as it looks like it may also be ripe for a paradigm shift. Past experience seems to indicate that when we have to to introduce artificial constructs (in this case, dark matter and dark energy) to maintain the coherence of our current model, it is usually a sign of major if not fatal flaw.

As a former food process engineer who agrees with Mr. Taubes that the hormone signaling is key, I find it interesting that the “palatability theory” never mentions the most widely used flavor enhancer – glutamic acid. An amino acid that targets the pancreas so specifically to produce insulin (sugar is not the only thing that causes the pancreas to release insulin), an amino acid that is the target of the drug topiramate to treat binge eating, an amino acid that targets the hypothalamus directly – the seat of hunger, and an amino acid – by virtue of being a neurotransmitter, that activates AMPK which basically then causes a feedback mechanism to kick in that causes mice to increase food intake and become “lazy” by reducing their activity to prevent running out of fuel, the very same amino acid that in animal studies makes the brain leptin resistant, and by the way causes gross obesity in the animals such that that is how they are created for obesity research. Fat and sugar have been around for a long time – fat longer than sugar, but extremely concentrated forms of glutamic acid have not. The fermentation process for making MSG was only cheap enough to use on a wide basis in 1967. When glutamate is broken down by the enzyme 85% of diabetics have antibodies to – GAD – it is turned into GABA which hits the same receptors in the brain as valium, Reward is part of the equation, but you cannot have a discussion, about the endocrine system, reward, or insulin without taking about the flavor enhancing elephant in the room that is mainly found in salty processed foods. Unfortunately the fact that it is neither a fat nor a carb has been keeping it out of the debate. Another thing to consider about obesity – is the influence of climate on brown fat composition. We are too comfortable temperature-wise compared to our forebears and that has an effect because energy burned as heat also is involved. Perhaps that is something to consider when comparing obesity rates of starving populations in various climates.

Hi Mr. Taubes,
Thank you for the insight, as always! (I think I have read nearly everything you have published on the carb/insulin hypothesis.)

I came across something interesting from Kurt Harris’ Archevore: http://www.archevore.com/panu-weblog/2011/9/29/jimmy-moore-inquires-about-safe-starches.html. In this post (3rd paragraph) he states that insulin is not the main fat storage regulator. “That would be leptin.” Ever since reading GC,BC a few years ago I have believed your hypothesis that insulin is the primary hormone for regulating fat metabolism, and have thus never given much thought to leptin. I am curious about your thoughts on leptin v. insulin concerning fat metabolism?

One point I reiterate is meats and cheeses are highly palatable, and yet they are not overeaten on a low carb diet and results in weight loss – food reward hypothesis rejected.

I, once, was on one of those non-palatable diet shakes he mentions (maybe not the same brand). They were high in sugar, but did NOT make me less hungry. In fact all I could think about was food and had to increase the number of cigarettes I smoked, and coffee drank, to curb the cravings. Sad.

I do believe that sugar can cause addictive cravings in the brain. But this does not mean that the insulin hypothesis is wrong, it may explain why we keep repeating these behaviours. But it does not explain WHY we get fat.

Gary’s argument to refute the palatability hypothesis is that the liquid fed to the four participants contained sugar, and sugar is palatable.
But does the fact that sugar was a big ingredient not also contradict the sugar-insulin hypothesis? When you grant that the obese patients in this study LOST weight on the diet despite eating this high-in-sugar stuff till they felt full?

Perhaps if the study only allowed set number of meals per day? (Regardless of whether participants were hungry in between? I’d be very curious to know if the participants felt hunger between their meals.

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Trackbacks

[...] Or a typical varied diet? If you ate nothing but Nutrament, described by the investigators at the time as a “bland liquid formula”, day in and day out, would you find it delicious? Would you wake up excited to drink it every morning? Would you choose a meal of this liquid over a steak, baked potato and salad? How about scrambled eggs, hash browns and coffee? Amazingly, Taubes argues that this would not have been a low-reward/palatability situation (35). [...]

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An eye-opening, paradigm-shattering examination of what makes us fat. In the New York Times best seller Good Calories, Bad Calories, acclaimed science writer Gary Taubes argues that certain kinds of carbohydrates—not fats and not simply excess calories—have led to our current obesity epidemic. Now he brings that message to a wider, nonscientific audience in this … [Read more]

[released as The Diet Delusion in the U.K.] In Good Calories, Bad Calories, Taubes tries to bury the idea that a low-fat diet promotes weight loss and better health. Obesity is caused, he argues, not by the quantity of calories you eat but by the quality. Carbohydrates, particularly refined ones like white bread and pasta, raise insulin … [Read more]

About

Gary Taubes (born April 30, 1956) is an American science writer. He is the author of Nobel Dreams (1987), Bad Science: The Short Life and Weird Times of Cold Fusion (1993), and Good Calories, Bad Calories (2007), which is titled The Diet Delusion in the UK. … [Read More...]

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Gary Taubes is available for media contacts and speaking engagements.
Feel free to send him a message.